The pedunculopontine nucleus (PPN) is located in the dorso-lateral part of the ponto-mesencephalic tegmentum. The PPN is composed of two groups of neurons: one containing acetylcholine, and the other containing non-cholinergic neurotransmitters (GABA, glutamate). The PPN is connected reciprocally with the limbic system, the basal ganglia nuclei (globus pallidus, substantia nigra, subthalamic nucleus), and the brainstem reticular formation. The caudally directed corticolimbic-ventral striatal-ventral pallidal-PPN-pontomedullary reticular nuclei-spinal cord pathway seems to be involved in the initiation, acceleration, deceleration, and termination of locomotion. This pathway is under the control of the deep cerebellar and basal ganglia nuclei at the level of the PPN, particularly via potent inputs from the medial globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. The PPN sends profuse ascending cholinergic efferent fibers to almost all the thalamic nuclei, to mediate phasic events in rapid-eye-movement sleep. Experimental evidence suggests that the PPN, along with other brain stem nuclei, is also involved in anti-nociception and startle reactions. In idiopathic Parkinson's disease (IPD) and parkinson plus syndrome, overactive pallidal and nigral inhibitory inputs to the PPN may cause sequential occurrences of PPN hypofunction, decreased excitatory PPN input to the substantia nigra, and aggravation of striatal dopamine deficiency. In addition, neuronal loss in the PPN itself may cause dopamine-r esistant parkinsonian deficits, including gait disorders, postural instability and sleep disturbances. In patients with IPD, such deficits may improve after posteroventral pallidotomy, but not after thalamotomy. One of the possible explanations for such differences is that dopamine-resistant parkinsonian deficits are mediated to the PPN by the descending pallido-PPN inhibitory fibers, which leave the pallido-thalamic pathways before they reach the thalamic targets.
Animal ; Basal Ganglia/cytology ; Human ; Mesencephalon/physiology* ; Mesencephalon/cytology ; Movement Disorders/etiology* ; Pons/physiology* ; Pons/cytology ; Thalamus/cytology

The ventral nucleus of the lateral lemniscus (VNLL) is an important nucleus in the central auditory pathway which connects the lower brainstem and the midbrain inferior colliculus (IC). Previous studies have demonstrated that neurons in the VNLL could respond to sound signal parameters. Frequency tuning curves (FTCs) of VNLL neurons are generally wider than FTCs of IC neurons, suggesting that the VNLL does not enhance abilities of frequency discrimination and coding. Two types of rate-intensity functions (RIFs) are found in the VNLL: monotonic and non-monotonic RIFs. Intensity-tuning of VNLL neurons are affected by the temporal firing patterns during processing and encoding intensity. There are multiple temporal firing patterns in VNLL neurons. Onset pattern has a precise timing characteristic which is well suited to encode temporal features of stimuli, and also very important to animal behavior including bat's echolocation. The VNLL accepts inputs from lower nuclei, uploads glycine inhibitory outputs to IC, and modulates response characteristics generating and acoustic signal processing of IC neurons. Recent research suggests that fast inhibitory projection from the VNLL may delay the first spike latency of IC neurons, and the delayed inhibitory projection from the VNLL may mediate the temporal firing patterns of IC neurons. But how inhibitory inputs from the VNLL integrate in IC, and how inhibitory inputs from the VNLL enhance the ability of detecting sound signal of IC neurons are not very clear and need more direct evidence at the level of neurons. These questions will help further understand the role of upload during IC processes acoustic signal, which are our research target in the future. This article reviews the current literature regarding the roles of the VNLL in sound signal processing and the auditory ascending transmission, including advances in the relevant research in our laboratory.
Acoustic Stimulation ; Animals ; Auditory Pathways ; Chiroptera ; Echolocation ; Neurons ; physiology ; Pons ; cytology

To access the role of the central nucleus of the amygdala (CeA) in the gustatory activity in the pontine parabrachial nucleus (PBN), the responses to four prototypical taste stimuli (NaCl, HCl, QH2SO4 and sucrose) in the PBN were observed before and after bilateral electrolytic lesion of the CeA in the urethane-anesthetized rat. Of 29 neurons, 14 were classified as NaCl-best, 9 as HCl-best, 3 as QH2SO4-best and 3 sucrose-best. After CeA lesions, the response rates to HCl and QH2SO4 were statistically higher across all PBN neurons (P<0.01). According to the best-stimulus category, the effects on the responses to HCl and QH2SO4 were similarly subjected to these modulations in NaCl-best, HCl-best and QH2SO4-best neurons. Correlation analysis indicated that the CeA lesion depressed the effect on the chemical selection between NaCl and QH2SO4. These findings suggest that the CeA plays an important role in the taste coding at the pontine level and it may be involved in mediating the feeding behavior via modulating the gustatory responses.
Amygdala ; injuries ; physiology ; Animals ; Electric Stimulation ; methods ; Female ; Male ; Pons ; cytology ; physiology ; Rats ; Rats, Sprague-Dawley ; Taste ; physiology

OBJECTIVEIt has been known that glial line-cell derived neurotrophic factor (GDNF) has the nutritional and protective effect in motor neurons. In this experiment, we investigated the character of GDNF mRNA expression in a facial nerve-striking model; combined with other scholars' experimental results; and analyzed what role GDNF plays in the regeneration process of injured motor nerves.

METHODSWe established a striking model in rabbit facial nerves with a striking gun with the striking velocity of 10 m/s and the total striking energy of 7.5 J. Then we detected the GDNF mRNA expression in facial neurons and axons with in situ hybridization on days 3, 7, 14 and 21 after striking. We counted the expression numbers of facial neurons and, compared with normal facial neurons and peripheral facial nerves.

RESULTSWe detected GDNF mRNA expression in the facial neurons from day 3 to day 21 after the facial nerve injured by striking. The peak of GDNF mRNA expression appeared on the 7th day, and then the expression number of facial neurons decreased gradually. A high level expression was also detected on day 21. GDNF mRNA expression was not detected neither in Schwann cells nor in normal facial neurons from the 3rd day to the 21st day.

CONCLUSIONGDNF is a kind of neurotrophic growing factor (NGF) that could be activated by injury. The character of GDNF mRNA expression was accordant to the process of nerve regeneration. These results showed that GDNF plays a very important role in the regeneration of injured motor nerves.

Animals ; Facial Nerve ; metabolism ; Facial Nerve Injuries ; metabolism ; Glial Cell Line-Derived Neurotrophic Factor ; In Situ Hybridization ; Male ; Motor Cortex ; metabolism ; physiology ; Nerve Growth Factors ; biosynthesis ; genetics ; Nerve Regeneration ; Neuronal Plasticity ; physiology ; Neurons ; metabolism ; Pons ; cytology ; metabolism ; physiology ; RNA, Messenger ; biosynthesis ; genetics ; Rabbits